A New Suppression Mechanism Against the Proliferation of Colorectal Cancer Cells
December 18, 2014
The research group of Okayama University Graduate School of Environmental and Life Sciences found that benzyl isothionate (BITC) has a suppression mechanism against the proliferation of colorectal cancer cells through the transcription factor NF-kappaB.
The findings were published online November 20, 2014 in the journal of Cell death & disease.
The prevalence of colorectal cancer is high in developed countries. Colorectal cancer is the leading cause of cancer death among Japanese women.
Accumulation of overexpressed beta-catenin in the nucleus activates the expression of its target genes such as cyclin D1. This transition contributes to cell proliferation and tumorigenesis in the development of colorectal cancers. Thus, targeting the beta-catenin/cyclin D1 pathway is a promising strategy for preventing the onset of colorectal cancer.
The transcription factor NF-kappaB has a major role in the antiproliferation effects of BITC in colorectal cancer cells. In addition, p53 tumor suppressor gene has a function of DNA repair, but p53 has been observed to be deficient in more than half of malignant tumors.
N. Abe, Prof. Y. Nakamura and their colleagues have shown that BITC is a novel type of antiproliferative agent that activates NF-kappaB and inhibits the activation of the beta-catenin/cyclin D1 pathway in p53-deficient colorectal cancer cells.
The findings reveal a new strategy for selective proliferation control.
The findings are expected to lead to the development of new drugs for cancer treatment and to contribute to the understanding of the function and safety of food derived compounds.
Contact Information:
Mototaka Senda, Ph.D.
US Representative
Intellectual Property Office, Organization for Research Promotion and Collaboration, Okayama University
Fremont, California USA
TEL: 1-510-797-0907
Email: takasenda@okayama-u.ac.jp
Y. Nakamura, Ph.D.
Graduate School of Environmental and Life Science, Okayama University, Okayama, Japan